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173 Cards in this Set
- Front
- Back
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What are indicators of Posterior Wall MI
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Large R in V1 V2
maybe Q in V6 mirror test |
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What are indicators of Lateral wall MI
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Q in I and AVL
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What are indicators of Inferior Wall MI
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Q in II, III, and AVF
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Where is the 'Best" place to have MI
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Inferior Wall MI (right ventricle damage)
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What are the indicators of Anterior wall MI
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Q in V1, V2, V3, or V4
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How is a bypass graft completed
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take vein from femoral attaching to arota to bypass the infaraction
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Obstruction of Right and Left bundle branches can lead to
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bradycardia
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What are eptoic phosi
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foregin tissues that generate own electrical impulses, can lead to problems such as atrial fibrilation
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Where is angiotensinogen produced
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produced and release by liver
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What happens when blood pressure drops or serum Na drops
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kidneys respond by releasing renin, renin cleaves off part of the plasma protein aniontension, forming ANGI
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After Angiotensin I is formed ACE is released from lungs
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and converted to Angiotensin II
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What is a zymogen
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Angiotensinogen (inactive precursor)
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Angiotensinogen is released by liver and floating in circulation, what 2 things cause Kindey to respond and release renin
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1. Low serum Na <130
2.Systolic BP <90 |
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Low serum Na<130
Systolic BP <90 the kindey thinks hypoperfused release renin |
YES
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Bradykinoinogen occurs along-side angiotensinogen, what changes bradykininogen
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Kallikrenin cahnges into Bradykinin
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What converts Bradykinin
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Kinase II converts brady kinin into Inactive gradments
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Where does Angiotenin II have effects on
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Vascular smooth mucle
CNS and PNS Adernal Cortex Kidneys Brain |
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What are AngII effects on vascular smooth muscle
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constrictions and increase Aterial BP
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What are AngII effect ofn CNS and PNS
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Smpathetic activatin vasoconstrtion increase CO, and increases Aterial BP
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What are Angiotensin II effects on adernal cortex
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Increase aldosterone secretion
increases Na Resportion, and kincrease Aterial BP |
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What are anigotensin II effects on kidneys
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increase Filrations Fractino, and decrease GFR,which lead to Increased Na+H20 retretion and increased BP
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What are Angiotensin II effects ofn brian
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Increase ADH and Increases THirst
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Increased ADH
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increases H20 absroption and leads to Na+ and Water retnion and icnreased BP
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Increase Thirst leads to
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Increase H20 ingestion, and increase Na+ and H20 reabsoprtion and increased arterial BP
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ACE not only converts Angiotensin I to Angiotensin II what also does it do
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Bradykinin, Substance P and enkephalin into inactive fragments
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What can convert Angiotensinogen to Angiogensin II without ACE
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TP factor Tonin and Cathespin
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There are high conc of ACE in lungs, and ACE is also bond to
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endothelium
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Increased CNS sympatethic outflow does what
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increases Cadiac activity
increases sympathatice actity to kidney and BV |
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Increased cardiac activity does what
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Activate B1 receptors
B2 receptors Alpha 1 receptrs |
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Increased sympatethci activty to kidney and BV does what
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activates Alpha 1 receptros, causing vasoconstrction and sodium retention
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Increased activity or overstimulation of B1, B2, and Alpha 1 receptor leads to
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myocytes death
increased arrthmias and Beta 1 receptor DOWN-regulation |
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What are bad effects of aldosterone
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Mg/K+ loss
Sympathetic activation/Parasympathic inbhition Myocardial Fibrosis |
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What does Mg and K loss lead to
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QT dispersion, ventricular arryhrtmias and cardic death
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Symppatehic activation and parasympatehtic inhibition leads to
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Tachycardia ischemia----then QT diserpsion and ventciular arrhtmias--death
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What does Myocaridal fibrosis lead to (more stiff heart)
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QT dispersion or ventricular arrhthmias
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What are aldosterone vascular effects
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aldosterone secreted primarly from renal medual and coranry arteries which stimulates fibroblasts, which increases amt of collagen and decreases complicance
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What is pre-load
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AKA left entrciular EDV, the amount of blood in the ventricle before it contracts
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Increaseing Na+ and H20 retentiona can increase
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PRE-loading
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What is afterload
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the presure that must be overcome for the ventricles to eject blood from the heart
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What is stroke volume
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vol ejected from heart after each contraction
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What is cardiac output
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volume of blood pumped out EACH ventricle in 1 min (TIME
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What is Cardiac Index
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vol blood per unit time per SA
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What is ejection fraction
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% of blood that is ejected from heart after a contraction
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What are 2 types of Echos
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1. Transespoheal (swallow best)
2. Transthoracic |
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More accurate than an Echo is MUGA--
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mutli-gated
acquistion scan |
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What is a Multi-gate acquistion scan
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Use TCH-99 label which bind to RBC and gives off gamma radiation
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What do DARK sport indicate on a MUGA
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dead tissue block
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What are physical signs of pre-load are
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HDPPS
Hepatomegaly Distended neck veins peripheal edema pulmonary crackles S3 or ventricular gallop |
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What is hepatomegaly
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central venous blood back up, and congestion in liver--caused by RIGHT-sided HF
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What is Distended neck veins
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volume overload, or reduction is Right-Side outflow creates back up of blood in jugular veins
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Peripheral edema is shows what
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right side outflow is decreased
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What is Pulmonary Crackles
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left-sided outflow is reduced (LEFT-SIDED HF
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What is S3 or ventricular gallop
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Result of atria ejectign blood into partiall filled ventricle indicating poor empting or volume overload
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PRELOAD is associated with
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volume overload
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What are physical signs of afterload
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Vascular diastolic PRESSURE
Pulse PRESSURE PULSES |
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The diastolic presure represent the pressure in the circulation that the heart has to overcome, the greater the afterload
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the greater the diastolic pressure
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What is Pulse pressure
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differance between systolic/and diastolic
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The more narrow the pulse pressure the
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greater the afterload
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The Swanz Ganz Catheter is inserted in goin, can get all pressure pts, and then is wedged deep in pulmonary to get
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Left ventricular EDV
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Increasing the stretch lenght of left atrium in sacromere length increases
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force of contraction and increases Stroke volume
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Sarcomere lenghtis an indirect measure of
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pre-load
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MAP=
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2x diastolic + systolic/3
or CO X SVR (systemic vascular resistance) |
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CO=
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SV X HR
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CO (cardiac output) noram range
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4-8 L/min
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CI (cardiac Index) normal range
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2.5-4 L/min/m2
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Pre-load indicators PAWP
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8-12
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After loadindicators
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Pulomary vascular resistance
Systemic vascular resistance |
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Pulmonary vascular resistance normally
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100-250 dynes/sec/cm
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Systemic vascular resisatnce normally
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800-1200 dynes/sec/cm
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What is the process by which ventricular size, shape and function are regulated by mechical, neurohormonal,and genetic factors
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remodeling
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What are 2 adaptive processes during normal growth or pathological damage
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hypertrophy
dialtion |
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What is Atheroscleriosis
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disease of the LARGE and medium sized arteries or Heart brain kidneys legs and other vital organs
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Atheroscleosis is characterized by formation
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of fibrous plaques in arterial walls
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Is atherosclerosis the leading cause of mortality and morbidity in developing countries
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YES
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Consequence of Atherosclerosis in brain arteries
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stroke
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Consequence of Atherosclerosis in cornary arteries
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stable angine
unstable angina MI |
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Consequene of Atherosclerosis in Leg arteries
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PVD (perihperal vascular artery disease)
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Atherosclerosis is the process that underlies
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Conary heart disase
Cerbrovascular disease Peripheral artery disease |
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What are risk factors for atherosclerosis
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Hyperlipidemia
smoking HTN age obesity sex diabetes family history stress |
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The artery wall consists of 3 layers
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1. Endothelail cells
2. Smooth muscle cells 3. Conncetive tissue (adventitia) |
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What are the 4 stages of atherosclerotic process
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1. Endothelial dysfunction
2. Fatty steak formation 3. Fibrous plaque formation 4. Plaque rupture (life long process) |
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What is the endotherlim
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thin layer of cells that line the interior surface of blood vessels
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Is the endotherlium the interface between blood and the rest of vessel wall
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YES
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What is the normal protective mechanism of endothelial cells for substances produces
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produces NO and Prostaglandin I2--vasodilates
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What are main actions of endotherlial cells
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anti-thrombotic
anti-inflammatory inhbits extraceullar growth |
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What types of substances are produced in endothelial dysfunction
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Angiotension II
Endothelin--vasoconstrict and decrease NO, and I2 |
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What are main actions of endothelial dysfunction
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Pro-thrombotic
Pro-inflammaotry Promote extracellaular growth |
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The process of atherosclerosis begisn when
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the endothelial lining is injured or damaged
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What are factors whic can injure the endothelium
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diabetes
smoking HTN hyperlipdiemia |
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As a result of endothelial injury what move out of the blood steam and through the lining of artery and INTO the artery wall
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lipoproteins and monocytes
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What are the INITAL lesion of atherosclerosis
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fatty steaks
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The fatty steaks are primarily made up of the following:
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lipoproteins
monocytes lymphoctes (T) |
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Where do lipoprotein, monocytes, and lymphocutes accumlate
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in space below endothelium
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What happens to the monocytes in the artery wall
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differentiate into macrophages
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What do machorphages do inside artery wall
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engulf liporteins(LDL) and form FOAM CELLS
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What are foam cells
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lipid rich cell and the HALLMARK of atherosclerosis
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Macrophages and foram cells screte what
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growth factros and cytokines
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What do growth factors and cytokines result in
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cell proliferation/inflammation and maxtrix degradation
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What happens in Fibrous Plaque formation
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foram cells acumulate, and smooth muscle cell MOVE into the endothelial cells
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The plaque conties to grow and begins to protude into teh lumen of the blood, and the fibrous plagques are overlayed by
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fibrous cap (doem of connetive tissue)
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As plaques protude out into the lumen of the vessel what happens to blood supply
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there is a decrease in blood supply to regions of heart, brain or peripheral arteries
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Fibrous Plaque formation results in ischemia (decrease O2 supply in Increase O2 demand, what happens as result of INcrease O2 demand
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1. Increase HR
2. Changes in Contractility 3. Intramyocardial wall tension |
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What causes chagnes in intramycardial wall tension
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1. changes in pressure/volume in ventricles (preload)
2. ressitance heart has to pump out against (afterload) |
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What arehte symtpoms of contary ischemia
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Chest pain
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Ischemia Heart disease result from imbalance of O2 supply and demand--what condiations are a result of this
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1. Stable/Unstable angina
2. MI (heart attack) |
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Unstable angina and MI are classified as
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acute contary syndromes (ACS)
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Plaques may occur thoughout the entire coronary vasculates, marowing of the vessel lumen, by what % may produce ischemia
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>50%
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Stable anignia is narrowing of vessel lumen
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>70%
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Where is worst place to have blockage
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Left Anterior Descending
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Definaiton of Stable Angina (exercise induced)
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reproducible pattern of chest pain, that occur secondary to narrowing of cornary arteries
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Stable angina is result of decrease O2 supply in present of increase O2 demand, so chest pain is relived by
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REST
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In stable angina the plaques are generally stable, meaning
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they have large lipid rich cores covered by THICK fibrous caps
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When does Unstable angina occur
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chest pain at REST or NOT releived by REST
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In unstable angina the plaques are UNSTABLE meaning
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the have large lipid rich cores covered by a THIN fibrous cap
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Why are thin fibrous caps dangerous
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mroe prone to rupture
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What happens when the fibrous cap ruptues (fissures)
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the contenst of the plaque seep out into the lumen
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The body sees the plaque as a "SITE OF INJURY", and what happens
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platetsl and blood cells are recuits, and aggregates, and more form a thrombus or clot
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Once platelts adherence to site of they are activated, what happens
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conforamtional change in glycoprotein IIb/IIIa surface recpetors on plateltes
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What happens in platelt aggreation
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platelts cross-link together through fibriongoen bridges between glycoprotein IIb/IIIa receptors
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Clots that partially occlude lumen of vessels RESULT in
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unstable angina
NON-ST segment elveation myocardial infeaction |
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Clots that COMPLETLY occlude the lumen result in
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ST segemtn evlenation MI
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In response to plaque ruptute, cells such as marcophages secrete inflammatory mediators into the circulation such as
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IL-1, IL6, TNF
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IL-1, IL-6 TNF sitmulate what
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C-reactive protein production in liver
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C reactive protein is a marker of
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cardiovascular risk
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A High Senstivity CRP test is available to determine risk, the higher the C-reactive protein, the
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higher the risk of having a first heart attack or recurrent events
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hs-CRP <1.0 mg/L=
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low CVD risk
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What is an average CVD
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1.0-3.0
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What is a high CVD risk
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>3.0
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C-reative protein plasama concentartion increase in response to inflammation so is it a NON-specific infalmmatory marker
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YES
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What other factors can increase CRP
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smoking
infection obesity arithritis |
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What are "HEAVY WEIGHTS" of MODIFIABLE CVD risk factors
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hyperlipidema
smoking hypertension diabetes |
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LDL (low density lipoprotein) is a major cause of
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injury to the endothelium and smooth muscle
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What happens when LDL becomes trapped in a vessel wall
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it undergoes oxidation
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What happens to Oxidized LDL
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is taken up by macrophages to form foam cells
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Oxidized LDL also stimulates what in vessel wall
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inflammatory processes in vessel walls
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HDL are associated with decrease CVD risk, what does HDL do
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HDL promotes lipid removal from the atheroscletoic plaque
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By promting cholesterol efflux HDL prevents
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the formation of foam cells in the vessel wall
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30% of CHD deaths are attribtable to smoking, a smokers risk for developing CVD is directly related to
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the number of cigaretes smoked per day
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What does smoking do to HDL and LDL levels
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smoking decrease HDL and increase LDL
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Smoking icrease carbon monoxide levels in blood can
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increase the risk for injury to endothelium
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Does smoking also constrict arteries and increases the tendency of blood to clot
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YES
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Angiotensin II is potent vasconstrictor and is elevated in pts with HTN, what else does angiotensin do to cause athersclerosis
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endothlial dysfuction
smooth muscle production in vessel wall inflammation of vessel wall, and oxidation of LDL in vessel wall |
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Diabetics without prior MI carry the same risk for conarary events as non-diabetics do
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YES
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Hyperglycemia and insulin resisatnce alters the function
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endothelial dysfuction cells
smooth muscle proliferation increases platelts agg and decreases plaque stability |
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What are other factors that may play a role in atherosclerosis
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Hmocyteine
Fibronigen Liprotein a LDL particle size |
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High levels of Homocysteine may directly injure the enjothelium what causes this
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deficiencies of folic acid, vit B6, or B12
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Does Fibrinogen promote blood clloting
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YES
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What is ideal LDL particle size
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Large bouanyt--is best b/c cant get into lining
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What is considered underwieght
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BMI <18.5
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What is consdier normal weight
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18.5-24.9
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What is consider overweight
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25.0-29.9
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What is considered Obsese
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Class I--30-34.9
Class II 35-39.9 Class III >40 |
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How do you calculate BMI
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weight in Kg/height in m2
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How do change from feet to m2
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height to inches
inches x 2.54 /100 and square |
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GUT FAT is worse than BUTT FAT
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YES
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Abdominal obesity is a wiast circufererence >
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102cm men
>88 cm in women |
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Visercal fat is most located in abdominal cavity and is MORE METABOLICALLY active than
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Subcutnaeous fat
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The traditional veiw of Adispose (fat) tissue was energy storage depo, protects vital organ and conserves body heat when is comtemporary view
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Fat is metabolically active endocrine organ which secrete cytokines and prothrombic markers into the circulation
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Obesity is a state of
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choronic low-grade inflammation
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What are inflammatory mediators released from adipose tissue
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IL-6, TNF, which increase CRP production in liver
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Infammaltory mediators may explain in part the relationship between obesity and
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CVD
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Metabolic syndrome is combination of medical disorders that increase risk for CVD, if you have >3 or equal to of the following you have metabolic syndrome
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Abd ovestiy
Increase TGs Decreased HDL Increased BP Increased Fasting Glucose |
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Two primary factors are thought to contribute to pathogenesis of metabolic syndrome:
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1. abd obesity
2. insuling resistance |
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What are metabolic complications of obesity
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free fatty acids
cytokines proinflammatory/prothrombotic mediators |
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A metabolic complication of obesity is increased Free Fatty acids
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Increased Free Fatty acids increases TG's production, decreases Insulin action, and Increases Glucose production
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What happens are result of cytokines
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decrease adipoentic (protective cytokine), and increase resistin
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What happesn as result of decrease adiponectin and increasing resistin
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decrease insulin sensitivity and pro-inflammatory states
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What happesn as result of proinfallmatory and prothromtic mediators (increase IL, TNF, and PAI-1)
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inflammation and prothrombotic state
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Insulin resistance is not a disease, but rather
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state that greatly increases the chance of a person developing several closely releated meatoblic abnormalites
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Obese person have >FFA, this results in
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increases Basal lipolyiss
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High levels of FFA overload
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muscle and liver, which enchanges insulin resistance
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FFA produced by visceral fat are diained into
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the portal vein and flood teh liver
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Increase Fatty acids to the liver causes
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Increased TG production, increased glucose production and decreased insulin action
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